CVS PBL lec#1 Dr. Akram Saleh Ischemic heart diseases

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Ischemic Heart Disease

The topics of the lectures are:

When to suspect IHD (manifestations)

Coronary circulation; basic concepts

Causes of IHD

Postponing Management of IHD to

lec#2

We will deal with two clinical cases in the

lecture; mentioned in Slides#3, 22.

Read it from the slides (case presentation)

and come back n_n" ..

o 65 yrs risk factor (over 45)

o Male risk factor

Now let's answer the question: What are

the possible ANATOMICAL causes of chest

pain?

- We should have a key in mind for

chest pain because of wide big list of

possible causes ranging from mild to

fatal. Anatomically from outside to

inside we have the following:

Musculoskeletal causes:

osteochondritis,

osteoarthritis of chest wall…

Pleuretic pain, inflammation

of the pleura.

Pericarditis.

Coronary artery narrowing

(IHD)

- The pain maybe referred in the

mediastinum; peptic ulcer,

gallbladder problems, cervical

spondylosis, reflux esophagitis…

- Massive pulmonary embolism maybe

the underlying cause; recall that a

SMALL pulmonary embolus will cause

pleuretic chest pain, whereas LARGE

embolus will cause symmetrical (not

sure of the word) severe pain

resembling MI.

- Aortic dissection maybe the

underlying cause; which may be

associated with aneurysm. Causes of

dissection are HTN, Marfan syndrome

Intimal tear blood goes from

the lumen to the wall separating

intima from media.

- Sudden Severe NOT life-threatening

may also exist: Acute pericarditis.

How to manage chest pain?

- We need to diagnose the before!

Analyze chest pain (site, nature..etc).

Usually local pain (can be pointed at

by finger) is not that serious, while

DIFFUSE pain is more serious and

needs attention. COMPRESSIVE pain

also needs attention and

characteristic for IHD (the patient

complains of “elephant on his

chest”!)

Let’s continue with our friend:

CASE #1

CVS PBL lec#1 Dr. Akram Saleh Ischemic heart diseases

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The pain is retrosternal, compressive in

nature, precipitated by walking (exertion),

relieved by rest, radiating to left shoulder

(or arm, hand, forearm, jaw, neck,

epigastrium..) associated with SWEATING,

nausea and vomiting.

Now we are pretty much certain that the

patient has STABLE ANGINA PECTORIS.

o The patient is Diabetic risk factor

o Smoker risk factor

This was the history… now we proceed to

Physical Examination (vital signs):

o ↑BP (160/100) this is high risk

factor (repeat the BP test to make

sure that it’s not high temporarily

because of physical stress).

o HR: 88 bpm normal

o Heart sounds: normal. (S3 may

evident in IHD)

Additional examinations we may do:

edema, chest crepitation.

Investigations and treatment will be

discussed next time. Let’s now talk

generally about MI.

Why does walking (exercise) cause the

pain?

- Normally the healthy coronaries are

responsive for increased demand and

can provide as much as 8 times the

supply at rest. But in the case;

demand is increased and coronaries

are narrowed by atherosclerotic

plaque the supply couldn’t be

increased as much IMBALANCE

(MISMATHC) between demand and

supply ensues ischemia to the

affected segment, which will initiate

many things; including acidosis, ↓pH,

radicals formation Stimulate nerve

fibers endings and cause pain

sensation.

Why is the pain diffuse?

- Because the innervation is segmental

(not isolated) .

Why does the pain radiate to the lt.

shoulder?

- Because they share the same

segment.

IMPORTANT HIGHLIGHTS:

The main cause of IHD is

atherosclerosis.

The most susceptible

arteries are the coronaries.

MI is the 1st cause of death

worldwide.

There is no specific

symptom for ↑BP, only

routine examination reveals

it.

Proper history taking: reach diagnosis

up to 65-70%

Physical examination: adds 10-20%

Investiations: add 10-20%

CVS PBL lec#1 Dr. Akram Saleh Ischemic heart diseases

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Investigations: include troponin levels,

cardiac enzymes, ECG… to be discussed

later.

The pain may develop on exertion in:

Epigastrium, jaw, intrascapular (maybe

confusing !), neck, shoulder, teeth. Maybe

even without chest pain!!

Elbow hand clenching of the patient

(slide#5) is suggestive for MI.

A 50 years old male is presented to ER with

severe chest pain for 2 hours. HR= 130 bpm

(tachycardia) , with low blood pressure,

auscultation reveals S3.

The 1st thing to think about as a clinician is

the common & dangerous…IHD.

o ↓BP+↑HR Bad prognosis.

o S3 (third sound) Bad prognosis.

Necrosis of a segment of myocardium

because of persistent complete ANOXIA

due to complete cessation of blood flow

“obstruction of the coronaries” will occur in

few minutes.

Usually the underlying cause of sudden IHD

is a thrombus which develops usually on

top of a rupture of atheroma.

The mechanism: Usually the atherosclerosis

is mild (30-40% obstruction) platelet

adhesion by molecules that act like glue

(vWF & glycoprotein IIb/IIIa) platelet

activation platelet aggregation.

- The whole process until now is called

1ry hemostasis.

Activation of coagulation system

formation of fibrin-rich thrombus

(activated by thrombin).

This thrombus may:

- Totally occlude the coronary artery

ST-segment elevation MI.

- or Sub-totally occlude the coronary

non-ST-segment elevation MI.

REMEMBER these words (were mentioned like a thousand times by the prof.):

CASE #2

↑

↑ ↑Small note

In Angina : >50% obstruction causes the pain.

CVS PBL lec#1 Dr. Akram Saleh Ischemic heart diseases

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take a look at slide #6 to recall

coronary arteries anatomy.

Normally there are potential collateral

channels between the coronaries, these

won’t open until stimulation by a potent

stimulant, the most important is ISCHEMIA.

If the obstruction was sudden MI

will occur (more common).

If the obstruction was gradual (days-

weeks) collateral circulation

develops no MI.

Thus; pts with history of angina will

have less necrosis than pts without!

That’s why MI is more dangerous in

the youth

{A comparison between MI and Angina}:

Usually MI pain comes at rest “wakes up the

patient”, while it come on exertion in

Angina.

Patient with MI is usually anxious, irritable,

sweaty, keeps moving in the bed trying to

find a comfortable position (no relief will

happen because it’s not position-related),

UNLIKE Angina (the patient doesn’t

move).

MI and Angina has the same site but MI

pain is more severe, persistent,

associated with N&V (nausea and

vomiting).

Now go to Slide#7:

As we’ve just mentioned, the IMBALANCE

between demand and supply in the

etiology of MI.

↑ HR, contractility, wall tension, muscle

mass, all increase the demand.

↓ coronary flow is the main cause of the

imbalance.

Hb level: ↓Hb level after severe anemia

may cause angina not related to

coronaries! “Hb carries 𝑂2 to

myocardium”.

Myocardial oxygen extraction:

In skeletal muscles; O2 extraction

INCREASES with exercise. Whereas in the

myocardium it does NOT, the only way to

increase supply is to increase coronary

flow because O2 extraction is already

high.

The most severe pain that a patient will ever

experience is MI, he feels like “I’m gonna die…” N&V and profuse sweating are results

of excessive vagal stimulation.

CVS PBL lec#1 Dr. Akram Saleh Ischemic heart diseases

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Risk Factors for Cardiovascular Disease are

divided into: modifiable (in wich we are

more concerned) and non-modifiable.

Read them from slide #9

Slides from 10-end aren’t that important,

the Prof. didn’t read them but he explained

two things:

- The 1st step in atherosclerosis is

endothelial dysfunction, which ends

in accumulation of lipids engulfed

by macrophages formation of

fibrous layer atherosclerotic

plaque.

- He explained the difference between

Stable and Unstable plaques

(Slide#24):

Unstable plaque (rupture-prone) has

more lipid pool, more inflammatory

cells, and thin fibrous cap.

Stable plaque has less lipid pool, more

smooth muscle cells, and thick fibrous

cap.

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